| RRC ID |
1394
|
| 著者 |
Yamaguchi N, Kubo C, Masuhiro Y, Lally ET, Koga T, Hanazawa S.
|
| タイトル |
Tumor necrosis factor alpha enhances Actinobacillus actinomycetemcomitans leukotoxin-induced HL-60 cell apoptosis by stimulating lymphocyte function-associated antigen 1 expression.
|
| ジャーナル |
Infect Immun
|
| Abstract |
We demonstrated previously that Actinobacillus actinomycetemcomitans leukotoxin (Ltx) is greatly able to induce apoptotic signaling in cells that are positive for lymphocyte function-associated antigen 1 (LFA-1), a cell receptor of Ltx. We investigated in this study whether inflammatory cytokines can regulate apoptosis of human leukemic HL-60 cells induced by Ltx. Of the cytokines tested, tumor necrosis factor alpha (TNF-alpha) significantly enhanced the Ltx-induced cell apoptosis. Northern and Western blotting analyses showed that TNF-alpha enhanced the expression of CD11a in the cells at both the mRNA and protein levels but did not do so for CD18 expression. TNF-alpha also enhanced the binding of Ltx to the cells. We also observed by measuring the mitochondrial transmembrane potential and the generation of superoxide anion that the cytokine enhanced Ltx-induced apoptosis in HL-60 cells. In addition, interleukin-1beta significantly enhanced Ltx-induced cell apoptosis, although the enhancing activity was lower than that of TNF-alpha. These stimulatory effects of both cytokines were also observed for human polymorphonuclear leukocytes. The ability of TNF-alpha to increase cell susceptibility to Ltx could be inhibited by preincubation of the cells with a monoclonal antibody against TNF receptor 1 but not by preincubation of the cells with a monoclonal antibody against anti-TNF receptor 2. Furthermore, the results of an assay of caspase 3 intracellular activity (PhiPhiLuxG1D2) showed that Ltx-induced caspase 3 activation was completely neutralized by CD18 antibody treatment, although significant neutralization was also observed with anti-CD11a antibody. Taken together, the results of the present study indicate that TNF-alpha acts as a potent stimulator of Ltx-induced HL-60 cell apoptosis via TNF receptor 1-mediated upregulation of LFA-1 expression.
|
| 巻・号 |
72(1)
|
| ページ |
269-76
|
| 公開日 |
2004-1-1
|
| DOI |
10.1128/IAI.72.1.269-276.2004
|
| PMID |
14688105
|
| PMC |
PMC343981
|
| MeSH |
Aggregatibacter actinomycetemcomitans / pathogenicity*
Aggregatibacter actinomycetemcomitans / physiology
Apoptosis*
Exotoxins / physiology*
HL-60 Cells
Humans
Interleukin-1 / pharmacology
Leukocytes, Mononuclear
Lymphocyte Function-Associated Antigen-1 / metabolism*
Receptors, Tumor Necrosis Factor / metabolism
Signal Transduction
Tumor Necrosis Factor-alpha / pharmacology
Tumor Necrosis Factor-alpha / physiology*
Up-Regulation
|
| IF |
3.201
|
| 引用数 |
13
|
|
WOS 分野
|
INFECTIOUS DISEASES
IMMUNOLOGY
|
| リソース情報 |
| ヒト・動物細胞 |
HL60(RCB0041) |
